A technique to convert a 3D printed cast used in the fabrication of an interim implant-supported crown into a definitive cast capturing the acquired emergence profile.

An esthetic peri-implant soft tissue contour is a critical element of the success of implant restorations in the esthetic zone. Once the optimal transmucosal soft tissue profile is formed, it needs to be accurately replicated on the master cast. This clinical technique involves the utilization of a silicone putty positioning index placed in the patient's mouth to accurately duplicate the external contour of teeth and soft tissue. By combining this positioning index with the implant-supported interim crown, the 3D-printed initial cast, which was used to fabricate the interim crown, can be conveniently and efficiently transformed into a definitive master cast.

Expression of Cre recombinase in chondrocytes causes abnormal craniofacial and skeletal development.

The cranial base synchondroses are growth centers that drive cranial and upper facial growth. The intersphenoid synchondrosis (ISS) and the spheno-occipital synchondrosis (SOS) are two major synchondroses located in the middle of the cranial base and are maintained at early developmental stages to sustain cranial base elongation. In this study, we report unexpected premature ossification of ISS and SOS when Cre recombinase is activated in a chondrocyte-specific manner. We used a Cre transgenic line expressing Aggrecan enhancer-driven, Tetracycline-inducible Cre (ATC), of which expression is controlled by a Col2a1 promoter. Neonatal doxycycline injection or doxycycline diet fed to breeders was used to activate Cre recombinase. The premature ossification of ISS and/or SOS led to a reduction in cranial base length and subsequently a dome-shaped skull. Furthermore, the mice carrying either heterozygous or homozygous conditional deletion of Tsc1 or Fip200 using ATC mice developed similar craniofacial abnormalities, indicating that Cre activity itself but not conditional deletion of Tsc1 or Fip200 gene, is the major contributor of this phenotype. In contrast, the Col2a1-Cre mice carrying Cre expression in both perichondrium and chondrocytes and the mice carrying the conditional deletion of Tsc1 or Fip200 using Col2a1-Cre did not manifest the same skull abnormalities. In addition to the defective craniofacial bone development, our data also showed that the Cre activation in chondrocytes significantly compromised bone acquisition in femur. Our data calls for the consideration of the potential in vivo adverse effects caused by Cre expression in chondrocytes and reinforcement of the importance of including Cre-containing controls to facilitate accurate phenotype interpretation in transgenic research.